School of Science & Technology

Role

Dr Richard Hulse is a sensory neurophysiologist whom investigates how the sensory nervous system regulates pain perception in health and disease. He contributes to undergraduate and postgraduate teaching across neuroscience, physiology and pharmacology. He is module lead for MSc research projects.

Career overview

Dr Hulse completed his PhD (2009) in the Pain Research Group at the University of Bristol. He investigated how sensory nerves can become activated following injury or disease. When sensory neurons are turned on this typically leads to pain and underlies how long lasting pain can develop in patients. This can occur in those patients who have cancer, diabetic, treated with chemotherapy or have arthritis. In a subsequent postdoctoral position at the University of Bristol, Dr Hulse extended his pain research portfolio and skillset by investigating the role of the vascular endothelial growth factor-A (VEGF) family in nociception. This encompassed research into how the sensory nerves and spinal cord sensory neurons control pain signals in response to VEGF signalling. In 2013, he was appointed as Senior Research Fellow in the Division of Cancer and Stem Cell Sciences at Nottingham University to investigate chemotherapy and cancer induced pain. Dr Hulse moved to Nottingham Trent University in 2017. Having spoken directly to diabetic and cancer patients who suffer from pain, he is directly aware of how this can impact upon quality of life and forms the basis for many of the research questions he wishes to answer. Understanding the neurophysiology responsible for controlling pain is crucial if we are to understand what goes wrong in chronic pain sufferers.

Research areas

Pain is usually a short lasting but uncomfortable experience that is controlled by the sensory nervous system. However, in chronic (long lasting) pain these systems go wrong ultimately leading to abnormal sensory complications such as prolonged and exacerbated pain. Pain is a unique experience to every organism, influenced by emotional experiences, treatment and/or disease. Neurons (peripheral and central nervous systems) are the epicentre of the pain signal, processing incoming sensory information. The sensory neurons act in harmony with an array of functionally distinct physiological systems (such as vascular and immune systems) to control our pain perception, which ultimately goes wrong in chronic pain states. We aim to understand these sensory neurophysiological systems to allow us to decipher alterations that cause pain.

Our work utilises an array of cellular and invivo rodent assays (models of disease and transgenics) to understand systems neuroscience in relation to pain. Nociceptive behavioural methodologies, invivo confocal microscopy and electrophysiological techniques are incorporated into these studies to allow greater understanding of how the sensory nervous system functions.

Current research areas include:

Diabetic neuropathic pain affects as many as 50% of patients suffering from sensory complications (burning pain, pins and needles). To date the efficacy and longevity of many current pain-killing drugs is poor. It is widely known that the plasticity of the sensory nervous system strongly underpins neuropathic pain through changes in the organisation, morphology and excitability of sensory neurons resulting in the summation and amplification of sensory signals. Our work to date highlights that in diabetics there are significant alterations in how the sensory neurons modulates sensory information. This arises due to changes in neurovascular coupling (Ved et al. 2018. J Physiol). We wish to establish how hyperglycaemia drives sensory neuron excitability to develop new treatment approaches for diabetic neuropathic pain.

Chemotherapy induced sensory neuropathy affects many cancer patients (~70%), both adults and children. The impact of disease or physical impact on neuronal systems leads to an array of sensory neuronal alterations; principally resulting in neuronal cell death and neural degeneration highlighted by nerve regression and neuronal apoptosis. These events affect neuronal signalling and neurotransmission, ultimately leading to the manifestation of pain. Unfortunately sensory neurons have a poor recovery/regeneration rate. This is likely to be attributable due to the loss of necessary growth/support factors such as VEGF-A. This is as a result of reduced transcriptional or translational processing indicating compromised repair processes. We are currently defining how chemotherapy can damage the sensory nervous system and activate the immune system but also establishing how this activates the sensory neurons to cause pain. By targeting these mechanisms we believe we can understand chemotherapy induced sensory neurodegeneration and pain, allowing us to effectively treat pain in the future.